Ocular Manifestations of Cutaneous T-Cell Lymphoma

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Article initiated by:
Pamela Davila-Siliezar, MD, Preston Tsang, Alexander W. Suh, Vina Ravichandran, Andrew G. Lee MD
All contributors:
Colleen Halfpenny, M.D., Michael T Yen, MD, Pamela Davila-Siliezar, MD
Assigned editor:
Joseph Giacometti, MD, Masako Chen, MD
Review:
Assigned status Up to Date
 by Michael T Yen, MD on April 28, 2024.


Background

Cutaneous T-Cell Lymphoma (CTCL) is characterized by the infiltration of malignant T lymphocytes into the skin. CTCL can further be divided into various subtypes, with mycosis fungoides (MF) and Sézary syndrome (SS) being the most common forms.[1] This rare type of non-Hodgkin lymphoma (NHL) primarily manifests as skin lesions, ranging from patches and plaques to tumors. CTCL can also lead to systemic symptoms such as fevers, chills, and fatigue. [2] According to the Leukemia and Lymphoma Society, CTCL accounts for approximately 4 percent of all cases of NHL and has shown to be twice as common in men as in women. Age is a risk factor for CTCL, with an average range of onset between 50 and 60 years, however, CTCL has been known to affect all ages.[3] The hallmark findings of CTCL are erythematous patches or plaques that progress into tumors in the advanced stages. The tumors present in an asymmetrical distribution that may be accompanied by pruritis, scaling, and ulceration. CTCL typically follows a chronic and indolent course, characterized by periods of remission and relapse. This varying disease course emphasizes the challenges in managing this malignancy.[4] We describe the ocular manifestations of CTCL which include: seborrheic blepharoconjunctivitis, cicatricial ectropion, meibomianitis, chalazia, and madarosis.[5]

Disease Entity

CTCL is an immune-mediated disorder involving the dysregulation of T cell function and immune surveillance mechanisms. The exact etiology remains elusive, although genetic predisposition, environmental factors, and viral infections may be contributory to its pathogenesis. According to a 15-year interval retrospective study only 1.95% of patients with CTCL have at least one attributable ophthalmic abnormality to the disease.[5] Treatment is difficult because of the progressive nature and propensity for disease recurrence.

Pathophysiology

Although there is no clear pathway, CTCL pathogenesis is hypothesized to be multifactorial with a combination of genetic, epigenetic, and immunological factors which contribute to all stages of malignant T cell clonal expansion.[6] Early stages of CTCL are composed of mostly benign cells with a small area of malignant T CD4+ cells.[7] Benign cells accumulate T helper cells (Th1) and interferon-gamma secreting CD8+ cells which prevent the growth of these malignant CD4+ cells.[8] In the advanced stages of CTCL, Th1 signaling defects coupled with a decrease benign regulating cells cause malignant T cell expansion.[7] As malignant CD4+ cells increase and produce a Th2 inflammatory immune response, the number of healthy T cells (CD4+ and CD8+) and natural killer cells decline and protection from healthy T cells declines, enabling disease progresses.[9]

The two common subcategories of CTCL are MF, representing 60% of CTCL cases, and SS, representing 5%.[8] Initially, MF resembles benign inflammatory conditions such as atopic dermatitis and plaque psoriasis. As the ratio of Th1 cells:Th2 cells shifts, MF progresses into erythroderma and can infiltrate lymph nodes and blood.[7],[10]  SS, the aggressive variant of MF, presents with a triad of erythroderma, lymph node enlargement, and malignant T cells in the skin, blood (Sezary cells), and lymph nodes.[11]

Presentation

Although ocular manifestations are found in a small percentage of patients with CTCL, eyelid and periorbital involvement have been reported in the advanced stages of the disease. [12],[13] The most common manifestations are seborrheic blepharoconjunctivitis and cicatricial eyelid ectropion.[14] CTCL ocular manifestations can vary in presentation but typically presents as erythematous, scaly plaques on the body and eyelids, especially in late-stage disease. 2 Diffuse thickening, edema, poikiloderma-like changes, atrophy and wrinkling suggest ocular MF, while ectropion suggests in Sezary syndrome. [15] Skin changes of the eyelid due to CTCL can cause irritation, inflammation, and susceptibility to Staphylococcus infections.[15] Symptoms of eyelid involvement can include erythema and edema, blurry vision, tearing, and discomfort. [16]

Cicatricial ectropion leads to lower eyelid margin inversion due to eyelid muscle weakness and scarring of the anterior lamella. This inversion leads to subsequent dryness which consequently results in redness, tearing, irritation.[17] In severe cases, cicatricial ectropion can cause corneal erosions, ulceration and ultimately vision loss if not treated emergently via surgical repair.[18] In early patients with CTCL, eyelid involvement is disguised as benign dermatitis.[19] Some studies have shown CTCL localizing to scars and keloids of previous trauma and/or surgeries.[20] While CTCL itself might not cause direct scarring of the eyelid, the disease might inhabit those areas of previous trauma and exacerbate the scarring, leading to cicatricial ectropion. Additional rarely reported ocular findings include meibomianitis, chalazia, and madarosis due to inflammatory eyelid involvement.[14]

Diagnosis

The diagnosis of CTCL involves a comprehensive integration of clinical evaluation, histopathological examination, immunophenotyping, and molecular studies. CTCL may be initially mistaken for benign dermatoses (e.g., eczema or psoriasis); however, characteristic features of CTCL include persistent and progressive erythematous patches and plaques with irregular borders as well as the presence of associated symptoms such as pruritis, pain, or tenderness. Skin biopsies and blood tests are essential in enabling clinicians to identify unique cellular features and specific biomarkers associated with CTCL and its subtypes, facilitating accurate diagnosis and guiding appropriate treatment strategies. The modified Severity-Weighted Assessment Tool (mSWAT) and Cutaneous Lymphoma International Prognostic Index (CLIPi) may also be effective clinical staging tools for assessing disease extent and guide treatment modalities.[21]

Ocular manifestations of CTCL may present with a wide variety of abnormalities, including eye redness, burning eyes, light sensitivity, blurred vision, dry eyes, itching, and eye discharge. Intensity of symptoms may fluctuate based on duration of disease, extent of invasion, and secondary infections.[22] Cicatricial ectropion can induce inducing symptoms of corneal exposure, ulceration, and vision impairment if left untreated.[5] Symptomatic patients should undergo thorough eye examinations by an ophthalmologist to assess for additional ocular manifestations of CTCL. Examinations should include, but are not limited to, evaluation for signs of: conjunctivitis, meibomianitis, blepharitis, and any alterations observed in the cornea or iris.

Ocular symptoms observed in CTCL may resemble those of other eye conditions, necessitating the exclusion of alternative causes. These may encompass infectious etiologies (e.g., keratitis), autoimmune disorders (e.g., sarcoidosis), other malignancies (e.g., Conjunctival Mucosa-Associated Lymphoid Tissue Lymphoma) as well as non-inflammatory conditions (e.g., Dry Eye Syndrome). A thorough differential diagnosis is imperative to accurately identify the underlying cause of ocular manifestations in patients with CTCL. Interestingly, optical coherence tomography (OCT) of CTCL patches (not ocular tissue) may be useful in detection of structural manifestations, demonstrating elongated hypo-reflective structures in the dermis, although further investigations are warranted.[23]

The improvement of ocular symptoms following treatment for CTCL (e.g., systemic methotrexate, photochemotherapy) can also serve as a valuable diagnostic indicator. If ocular conditions respond positively to these therapies, it may aid in the diagnosis.[24] Timely diagnosis and intervention play a pivotal role in preventing further complications and maintaining optimal eye health.

Differential Diagnosis

  • Conjunctivitis
  • Ocular surface disease (e.g., Dry Eye Syndrome)
  • Conjunctival Mucosa-Associated Lymphoid Tissue Lymphoma
  • Conjunctival Squamous Cell Carcinoma
  • Infectious Keratitis/Conjunctivitis
  • Ocular Rosacea
  • Chronic Blepharitis
  • Ocular Adnexal Lymphoma
  • Sarcoidosis
  • Ocular manifestations of psoriasis

Management

Overall, the management options for ocular manifestations of CTCL varies widely based on which of the manifestations occurs in each individual patient with CTCL. The treatment options should be tailored to specific manifestations and their severity. It is likely that the best outcome for CTCL ocular manifestations will involve interdisciplinary teams comprising of internists, ophthalmologists, reconstructive surgeons, and dermatologist collaborating to achieve the greatest relief of symptoms and preserve the vision of the patient.

Seborrheic Blepharoconjunctivitis Management

Seborrheic blepharoconjunctivitis is the most common ocular manifestation of CTCL. The mainstay treatment of blepharoconjunctivitis is careful lid hygiene. This involves a hyperthermic lid compress for 5-10 min, lid margin massage 3-5 twice a week, and eyelash scrub with baby shampoo. The goals of these management plans are to express the oil and remove debris. Regardless of an acute exacerbation or not, patients are encouraged to retain lid hygiene due to the chronic nature of the disease process. Following lid hygiene, topical antibiotic ointment (e.g., erythromycin or bacitracin) should be offered for 4-8 weeks to achieve the greatest control. [5],[25]

For patients with posterior blepharitis, which is more difficult to control with conservative lid treatment and topicals, oral tetracyclines or macrolides may be used. In addition, tetracyclines ability for lipase inhibition, anti-inflammatory properties, and lipid regulation may provide improvements seen in blepharoconjunctivitis due to S. aureus and S. epidermidis. Providers should be aware of potential photosensitization, gastrointestinal symptoms, and hypersensitivity of tetracyclines during administration.[25]

Cicatricial Ectropion Management

CTCL is believed to lead to cicatricial lower lid ectropion by chronic inflammation and involutional changes. There is a vertical shortening and/or scarring of the anterior lamella of the eyelid that may be repaired via surgery.[17] Some techniques for repair include: lengthening of the anterior lamella with transition flaps, full-thickness free skin grafts, z-plasty, lateral tarsal strip, medial ectropion repair, and filler injections.[26]

Surgical correction of cicatricial ectropion poses a challenge to surgeons because of variation in scarring, location, and degree of lid laxity. Techniques for scar release include: z-plasty, myocutaneous flap, and full-thickness skin grafts. Depending on the amount of lid laxity present after scar release, there may be an indication to perform a lateral tarsal strip procedure. Medial lid laxity is an indication for the medial spindle procedure.[26]Another consideration when surgically correcting cicatricial ectropion is the use of tension vectors parallel to the lid margin. Tension vectors must be parallel to the lower eyelid free margin to mitigate perpendicular tension which can pull down the lid and limit repair efficacy.[26]

Novel treatment of cicatricial ectropion with hyaluronic acid filler has been explored as an alternative to surgical correction. The filler works by stretching the tethered, scarred down skin and expanding the tissue to correct the shortened anterior lamella. Hyaluronic acid is a known safe and effective filler for facial wrinkles. It has been widely used in lower lid and cheek hollows and lasts 12-18 months. In a study by Dr. Feza, fifteen patients underwent cicatricial ectropion correction with hyaluronic acid filler and followed for one year.[27] Patients were injected in a linear threading fashion from lateral to medial with 1cc of hyaluronic acid along the inferior orbital rim and in the intraciliary region.  Eleven of those patients saw significant improvement without major complications. Twelve patients had bruising and three had small filer lumps treated with massage.[27]

Meibomianitis Management

Traditional treatment of meibomianitis consists of warm compresses and lid hygiene for removal of meibum. The addition of antibiotics or anti-inflammatory agents can help relieve dysfunctioning meibomian glands.[28] Despite having numerous treatment options, complete relief of symptoms associated with meibomian gland dysfunction is difficult to achieve. Additional treatment options such as intraductal meibomian gland probing, LipiFlow thermal pulasation system, azithromycin, oral supplementation with omega-3 essential fatty acids, and cyclosporin A show promise for maximal symptomatic relief. [29]

Intraductal meibomian gland probing allows for mechanical dilation and opening of the natural orifices and ducts of the meibomian gland to remove abnormal meibum secretions. The probe passes through the orifices perpendicular to the lid margin. In one study, Maskin reported 24 out of 25 cases which had immediate relief of symptoms after probing, and 25 out of 25 cases had relief after four weeks. The most notable downside was the mid-procedure discomfort experienced by patients which was resolved with topical lidocaine. Orifice hemorrhage caused by entrance of the probe was self-resolving in all patients.[30]

LipiFlow relieves obstruction of the meibomian gland and treats meibomianitis by applying heat to both the upper and lower palpebral conjunctival surface in addition to applying pressure to express the meibomian gland. The lid warmer vaults the cornea to heat the upper and lower lids simultaneously, while the eye cup contains an inflatable bladder to compress the glands and express meibum. Downsides include moderate conjunctival vascular injection, ocular burning symptoms, and eyelid pain, all of which resolved after 4 weeks post treatment.[31] In a study done by Greiner, a single twelve minute LipiFlow treatment resulted in up to nine months of normal meibomian gland function and relief of symptoms.[32] Of note, there are multiple devices similar to the LipiFlow such as the MiBo Thermaflow, BlephEx, Intense Pulse Tx, KCL1100 etc. that also aim to liquify and express meibum and have been shown to be effective.[33]

In a double-masked open-label clinical trial assessing efficacy of azithromycin compared to doxycycline for meibomian gland dysfunction, it was found that both oral azithromycin and doxycycline showed improvement of symptoms of meibomian gland dysfunction. However, in the 110 patients randomly assigned to oral 5-day azithromycin (500 mg on day 1 and then 250 mg/day) or 1-month doxycycline (200 mg/day), the 5-day oral azithromycin was favored based on overall more effective clinical improvement with a shorter treatment period.[34]

Lastly, studies including nutritional support with omega-3 essential fatty acids have been reported to show improvement in meibomian gland dysfunction. It is hypothesized that the breakdown of omega-3 essential fatty acids help suppress inflammation by inhibiting inflammation promoting omega-6 fatty acids, thus leading to decreased inflammation of the eyelid. Additionally, the omega-3 essential fatty acids are hypothesized to alter the properties of meibum, therefore stabilizing and suppressing inflammation.[35]

Chalazia Management

Chalazia, one of the most common eye conditions in patients with CTCL, presents as a mass lesion on the eyelid caused by blockage of the meibomian or zeis glands, is treated similarly to meibomian gland dysfunction. In a study exploring the various treatment modalities, it was agreed that treatment varies from clinician to clinician, with treatments ranging from compresses, lid hygiene, local antibiotic ointment, steroid injections, surgery, to experimental methods such as Botox, tarsal trephination, and CO2 laser or cryogenic action.[36] At the end of the review of chalazia management methods, it was highlighted that treating chalazia conservatively with hot compress had lower resolution rate with increased recurrence rate. The highest resolution rate management was through intralesional triamcinolone and incision and curettage. When compared to subcutaneous administration of triamcinolone acetonide (TA) and incision curettage, conservative treatments have much lower rates of resolution. Reported resolution of chalazia with subcutaneous injection of triamcinolone was a high of 94%.[37] To treat the chalazia, the injection is delivered transconjunctivally or transcutaneously. A 0.2-0.4mL injection of 4 mg/mL of Triamcinolone acetonide should be injected to effectively treat the chalazia.[38] A side effect of subcutaneous TA injection was the potential for eyelid skin hypopigmentation post treatment. [39]

Surgical treatment with incision and curettage revealed a highest resolution rate of 76% in a study comparing intralesional triamcinolone acetonide and incision and curettage treatment for primary chalazia.[40] The procedure is a minor surgery requiring local anesthesia and involves a vertical incision made on the tarsal mucosa wherein the lipogranulomatous content is drained with a curette. Patients are advised to apply topical antibiotics post op three times a day for five days.[38]

Madarosis Management

Madarosis is the loss of eyebrows or eyelashes that can be scarring or non-scarring. The management technique varies between tattooing, surgery, follicular unit transplantation, and grafting.[41] Amongst the spectrum of management, surgical management has been proven to be the most effective method for managing madarosis.[41] Other common procedures include follicular unit transplantation for eyebrows and eyelash grafting.  Follicular unit transplants harvest donor strips from below the nuchal ridge or lower part of the scalp.[42] Eyelash transplantation involves using a strip composite graft from the eyebrow because of the lash and brow hair similarities.[43]

In addressing ocular manifestations of Cutaneous T-cell Lymphoma (CTCL), effective management frequently necessitates a collaborative effort between dermatologists and ophthalmologists. Given the prevalence of ocular involvement in CTCL cases, proactive ocular screening is essential, even in the absence of overt symptoms. Treatment strategies should be individualized according to the severity of ocular symptoms. As our understanding of the underlying cellular and autoimmune mechanisms driving ocular manifestations in CTCL improves, there is a promising shift towards more targeted interventions aimed at preserving visual function and mitigating patient burden.

References

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  2. ↑ Semaan S, Abel MK, Raffi J, Murase JE. A clinician’s guide to cutaneous T-cell lymphoma presenting as recalcitrant eczematous dermatitis in adults. Int J Womens Dermatol. 2021;7(4):422-427. doi:10.1016/j.ijwd.2021.04.004
  3. ↑ Cutaneous T-Cell Lymphoma | Leukemia and Lymphoma Society. Accessed March 14, 2024. https://www.lls.org/booklet/cutaneous-t-cell-lymphoma
  4. ↑ Hague C, Farquharson N, Menasce L, Parry E, Cowan R. Cutaneous T-cell lymphoma: diagnosing subtypes and the challenges. Br J Hosp Med Lond Engl 2005. 2022;83(4):1-7. doi:10.12968/hmed.2021.0149
  5. ↑ 5.0 5.1 5.2 5.3 Cook BE, Bartley GB, Pittelkow MR. Ophthalmic abnormalities in patients with cutaneous T-cell lymphoma. Ophthalmology. 1999;106(7):1339-1344. doi:10.1016/S0161-6420(99)00721-6
  6. ↑ Bagherani N, Smoller BR. An overview of cutaneous T cell lymphomas. F1000Research. 2016;5:F1000 Faculty Rev-1882. doi:10.12688/f1000research.8829.1
  7. ↑ 7.0 7.1 7.2 Patil K, Kuttikrishnan S, Khan AQ, et al. Molecular pathogenesis of Cutaneous T cell Lymphoma: Role of chemokines, cytokines, and dysregulated signaling pathways. Semin Cancer Biol. 2022;86:382-399. doi:10.1016/j.semcancer.2021.12.003
  8. ↑ 8.0 8.1 Bobrowicz M, Fassnacht C, Ignatova D, Chang YT, Dimitriou F, Guenova E. Pathogenesis and Therapy of Primary Cutaneous T-Cell Lymphoma: Collegium Internationale Allergologicum (CIA) Update 2020. Int Arch Allergy Immunol. 2020;181(10):733-745. doi:10.1159/000509281
  9. ↑ Vakiti A, Padala SA, Singh D. Sezary Syndrome. In: StatPearls. StatPearls Publishing; 2024. Accessed March 16, 2024. http://www.ncbi.nlm.nih.gov/books/NBK499874/
  10. ↑ Vaidya T, Badri T. Mycosis Fungoides. In: StatPearls. StatPearls Publishing; 2024. Accessed March 16, 2024. http://www.ncbi.nlm.nih.gov/books/NBK519572/
  11. ↑ Varghese MT, Alsubait S. T-Cell Lymphoma. In: StatPearls. StatPearls Publishing; 2024. Accessed March 16, 2024. http://www.ncbi.nlm.nih.gov/books/NBK564354/
  12. ↑ Periorbital Involvement in Early Stage Mycosis Fungoides. doi:10.2340/00015555-2676
  13. ↑ Jusufbegovic D, Char DH. Clinical Variability of Ocular Involvement in Mycosis Fungoides. JAMA Ophthalmol. 2015;133(3):341-343. doi:10.1001/jamaophthalmol.2014.5223
  14. ↑ 14.0 14.1 Leib ML, Lester H, Braunstein RE, Edelson RL. Ocular findings in cutaneous T-cell lymphoma. Ann Ophthalmol. 1991;23(5):182-186.
  15. ↑ 15.0 15.1 Baykal C, Atci T. Eyelid involvement of primary cutaneous lymphomas: A clinical perspective. Australas J Dermatol. 2023;64(4):463-475. doi:10.1111/ajd.14131
  16. ↑ Colossi CG, Mondadori J, Barreto PKM, Valença FM, Duquia R, Vilela MAP. Mycosis Fungoides: Analysis of Ophthalmologic Findings in a Series of Cases. Case Rep Dermatol Med. 2019;2019:e2380598. doi:10.1155/2019/2380598
  17. ↑ 17.0 17.1 Comer MB, Wharton SB, Hughes DS. Cicatricial ectropion in mycosis fungoides and sézary syndrome: Successful surgical repair. Ann Ophthalmol. 2000;32(3):196-198. doi:10.1007/s12009-000-0052-z
  18. ↑ Ozgur O, Kaufman EJ. Ectropion. In: StatPearls. StatPearls Publishing; 2024. Accessed March 20, 2024. http://www.ncbi.nlm.nih.gov/books/NBK441929/
  19. ↑ Aldrees SS, Zoroquiain P, Alghamdi SA, Logan PT, Callejo S, Burnier MN. Conjunctival Involvement of T-Cell Lymphoma in a Patient with Mycosis Fungoides. Case Rep Ophthalmol Med. 2016;2016:4786498. doi:10.1155/2016/4786498
  20. ↑ Ehsani AH, Kamyab-Hesari K, Noormohammadpour P, Mahmoudi H, Razavi Z. An enlarging scaly plaque localized on the previous keloid of the chest. Clin Case Rep. 2020;8(2):265-268. doi:10.1002/ccr3.2650
  21. ↑ Modified Severity-Weighted Assessment Tool (mSWAT). Cutaneous Lymphoma Foundation. Accessed March 14, 2024. https://www.clfoundation.org/modified-severity-weighted-assessment-tool-mswat
  22. ↑ Pulitzer M. Cutaneous T-cell Lymphoma. Clin Lab Med. 2017;37(3):527-546. doi:10.1016/j.cll.2017.06.006
  23. ↑ Ring HC, Stamp IMH, Jemec GBE. Imaging Cutaneous T-Cell Lymphoma with Optical Coherence Tomography. Case Rep Dermatol. 2012;4(2):139-143. doi:10.1159/000340010
  24. ↑ Colossi CG, Mondadori J, Barreto PKM, Valença FM, Duquia R, Vilela MAP. Mycosis Fungoides: Analysis of Ophthalmologic Findings in a Series of Cases. Case Rep Dermatol Med. 2019;2019:1-4. doi:10.1155/2019/2380598
  25. ↑ 25.0 25.1 McCULLEY JP, Dougherty JM. Blepharitis Associated with Acne Rosacea and Seborrheic Dermatitis. Int Ophthalmol Clin. 1985;25(1):159.
  26. ↑ 26.0 26.1 26.2 Kooistra LJ, Scott JF, Bordeaux JS. Cicatricial Ectropion Repair for Dermatologic Surgeons. Dermatol Surg. 2020;46(3):341. doi:10.1097/DSS.0000000000002150
  27. ↑ 27.0 27.1 Fezza JP. Nonsurgical Treatment of Cicatricial Ectropion with Hyaluronic Acid Filler. Plast Reconstr Surg. 2008;121(3):1009. doi:10.1097/01.prs.0000299382.31856.d8
  28. ↑ Olson MC, Korb DR, Greiner JV. Increase in tear film lipid layer thickness following treatment with warm compresses in patients with meibomian gland dysfunction. Eye Contact Lens. 2003;29(2):96-99. doi:10.1097/01.ICL.0000060998.20142.8D
  29. ↑ Qiao J, Yan X. Emerging treatment options for meibomian gland dysfunction. Clin Ophthalmol Auckl NZ. 2013;7:1797-1803. doi:10.2147/OPTH.S33182
  30. ↑ Maskin SL. Intraductal meibomian gland probing relieves symptoms of obstructive meibomian gland dysfunction. Cornea. 2010;29(10):1145-1152. doi:10.1097/ICO.0b013e3181d836f3
  31. ↑ Lane SS, DuBiner HB, Epstein RJ, et al. A new system, the LipiFlow, for the treatment of meibomian gland dysfunction. Cornea. 2012;31(4):396-404. doi:10.1097/ICO.0b013e318239aaea
  32. ↑ Greiner JV. A single LipiFlow® Thermal Pulsation System treatment improves meibomian gland function and reduces dry eye symptoms for 9 months. Curr Eye Res. 2012;37(4):272-278. doi:10.3109/02713683.2011.631721
  33. ↑ Gupta PK, Periman LM, Lain E, et al. Meibomian Gland Dysfunction: A Dermatological Perspective on Pathogenesis and Treatment Outlook. Clin Ophthalmol. 2021;Volume 15:4399-4404. doi:10.2147/OPTH.S327407
  34. ↑ Kashkouli MB, Fazel AJ, Kiavash V, Nojomi M, Ghiasian L. Oral azithromycin versus doxycycline in meibomian gland dysfunction: a randomised double-masked open-label clinical trial. Br J Ophthalmol. 2015;99(2):199-204. doi:10.1136/bjophthalmol-2014-305410
  35. ↑ Macsai MS. The role of omega-3 dietary supplementation in blepharitis and meibomian gland dysfunction (an AOS thesis). Trans Am Ophthalmol Soc. 2008;106:336-356.
  36. ↑ Tashbayev B, Chen X, Utheim TP. Chalazion Treatment: A Concise Review of Clinical Trials. Curr Eye Res. 2024;49(2):109-118. doi:10.1080/02713683.2023.2279014
  37. ↑ Chung CF, Lai JSM, Li PSH. Subcutaneous extralesional triamcinolone acetonide injection versus conservative management in the treatment of chalazion. Hong Kong Med J Xianggang Yi Xue Za Zhi. 2006;12(4):278-281.
  38. ↑ 38.0 38.1 Goawalla A, Lee V. A prospective randomized treatment study comparing three treatment options for chalazia: triamcinolone acetonide injections, incision and curettage and treatment with hot compresses. Clin Experiment Ophthalmol. 2007;35(8):706-712. doi:10.1111/j.1442-9071.2007.01617.x
  39. ↑ Ho SY, Lai JSM. Subcutaneous steroid injection as treatment for chalazion: prospective case series. Hong Kong Med J Xianggang Yi Xue Za Zhi. 2002;8(1):18-20.
  40. ↑ Ben Simon GJ, Rosen N, Rosner M, Spierer A. Intralesional triamcinolone acetonide injection versus incision and curettage for primary chalazia: a prospective, randomized study. Am J Ophthalmol. 2011;151(4):714-718.e1. doi:10.1016/j.ajo.2010.10.026
  41. ↑ 41.0 41.1 Kumar A, Karthikeyan K. Madarosis: A Marker of Many Maladies. Int J Trichology. 2012;4(1):3-18. doi:10.4103/0974-7753.96079
  42. ↑ Gandelman M, Epstein JS. Hair transplantation to the eyebrow, eyelashes, and other parts of the body. Facial Plast Surg Clin N Am. 2004;12(2):253-261. doi:10.1016/j.fsc.2003.12.002
  43. ↑ Kasai K. Eyelash reconstruction with strip composite eyebrow graft. Ann Plast Surg. 2008;60(6):649-651. doi:10.1097/SAP.0b013e3181461e3a
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